Evidence map›Paper›PMID 28928419›Full record

ArticleScientific reports2017

The histone deacetylase SIRT6 blocks myostatin expression and development of muscle atrophy.

Sadhana A Samant, Abhinav Kanwal, Vinodkumar B Pillai, Riyue Bao, Mahesh P Gupta

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 47 citations in OpenAlex.

  1. Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026
    Review
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  8. Effects of Atmospheric Ammonia on Skeletal Muscle Growth in Broilers.Animals : an open access journal from MDPI · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Article
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  14. Article
  15. Article
  16. NADMolecular and cellular biochemistry · 2022
    Review
  17. Article
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  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Sadhana A SamantDepartment of Surgery, The Pritzker School of Medicine, The University of Chicago, Chicago, IL, 60637, USA.
Abhinav KanwalDepartment of Surgery, The Pritzker School of Medicine, The University of Chicago, Chicago, IL, 60637, USA.
Vinodkumar B PillaiDepartment of Surgery, The Pritzker School of Medicine, The University of Chicago, Chicago, IL, 60637, USA.
Riyue BaoCenter for Research Informatics, Biological Sciences Division, The University of Chicago, Chicago, IL, 60637, USA.ORCID 0000-0002-6105-1704
Mahesh P GuptaDepartment of Surgery, The Pritzker School of Medicine, The University of Chicago, Chicago, IL, 60637, USA. mgupta@surgery.bsd.uchicago.edu.
University of Chicago · US

Funding

Blocking cardiac toxicity of anticancer drugsR01HL117041 · NHLBI · UNIVERSITY OF CHICAGO · PI GUPTA, MAHESH P · 2013 to 2016
$1.8M
Activation of sirtuins to prevent adverse cardiac remodeling after CABGR01HL111455 · NHLBI · UNIVERSITY OF CHICAGO · PI GUPTA, MAHESH P · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL111455NHLBI NIH HHS R01 HL117041
6 · The paper itself

Abstract

Muscle wasting, also known as cachexia, is associated with many chronic diseases, which worsens prognosis of primary illness leading to enhanced mortality. Molecular basis of this metabolic syndrome is not yet completely understood. SIRT6 is a chromatin-bound member of the sirtuin family, implicated in regulating many cellular processes, ranging from metabolism, DNA repair to aging. SIRT6 knockout (SIRT6-KO) mice display loss of muscle, fat and bone density, typical characteristics of cachexia. Here we report that SIRT6 depletion in cardiac as well as skeletal muscle cells promotes myostatin (Mstn) expression. We also observed upregulation of other factors implicated in muscle atrophy, such as angiotensin-II, activin and Acvr2b, in SIRT6 depleted cells. SIRT6-KO mice showed degenerated skeletal muscle phenotype with significant fibrosis, an effect consistent with increased levels of Mstn. Additionally, we observed that in an in vivo model of cancer cachexia, Mstn expression coupled with downregulation of SIRT6. Furthermore, SIRT6 overexpression downregulated the cytokine (TNFα-IFNγ)-induced Mstn expression in C2C12 cells, and promoted myogenesis. From the ChIP assay, we found that SIRT6 controls Mstn expression by attenuating NF-κB binding to the Mstn promoter. Together, these data suggest a novel role for SIRT6 in maintaining muscle mass by controlling expression of atrophic factors like Mstn and activin.

Indexed as

Up-RegulationActivin Receptors, Type IIActivinsAngiotensin IIAnimalsHumansMiceMice, KnockoutMuscle, SkeletalMuscular AtrophyMyocardiumMyostatinNF-kappa BRatsResponse ElementsSirtuinsActivin Receptors, Type IIactivin receptor type II-BActivinsAngiotensin IIMstn protein, mouseMyostatinNF-kappa BSirt6 protein, mouseSirtuins

Identifiers

PMID28928419
PMCPMC5605688
OpenAlexW2754444406

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.